Converging evidence from animal and human subject studies supports the hypothesis that endogenous stress hormones (e.g., epinephrine, cortisol) interact with the amygdala to modulate explicit memory consolidation for emotionally arousing events. Our recent work involving human subjects has developed this theoretical framework in several ways. Most relevant to this proposal, we found that post-learning stress hormone activation does not uniformly enhance long-term memory consolidation; rather, that it interacts with the degree of arousal at initial encoding of a stimulus to modulate consolidation. We have also demonstrated a relationship between spontaneous, intrusive recollections after viewing emotional films and the strength of long-term memory for the films. Finally, we have uncovered pronounced sex-related influences on brain and hormonal mechanisms of emotional memory. The primary goal of this proposal is to conduct cognitive and neurobiological studies to better understand brain and hormone mechanisms regulating consolidation of emotional memory. The specific experimental aims build on our recent findings, and fall into one of three general sections. The first section will examine stress- and sex-hormone mechanisms underlying enhanced memory consolidation induced by cold pressor stress. The second section will examine adrenocortical and adrenomedullary involvement in the relationship we have found between spontaneous, intrusive recollections after viewing emotional films and strength of memory for the films. The third section will use PET scanning and Structural Equation Modeling ("Path Analysis") to identify brain regions with which the amygdala interacts to influence emotional memory. Each of these studies will be conducted independently on women and men. Collectively, these investigations should substantially advance our understanding of how brain and hormone systems interact to regulate explicit memory consolidation for emotionally stressful events. In so doing they should further close the gap that exists between our knowledge of "normal" brain memory mechanisms for emotional events, and of pathological mechanisms following emotionally traumatic experiences that are central to the etiology of disorders such as Clinical Depression and Posttraumatic Stress Disorder.